Autologous, lentivirally transduced second-generation CAR T-cell therapy (CD4+ and CD8+) targeting B7-H3 (CD276), EGFR806 epitope on EGFR/EGFRvIII, HER2 (ERBB2), and IL13Rα2 via an IL13-zetakine design; administered locoregionally via intraventricular catheter to drive CAR-mediated cytotoxic killing of CNS tumor cells and mitigate antigen escape.
Autologous CD4+/CD8+ T cells are lentivirally engineered to express four second-generation CARs targeting B7-H3 (CD276), the tumor-restricted EGFR806 epitope on EGFR/EGFRvIII, HER2, and IL13Ra2 (via an IL13-zetakine design). Following locoregional intraventricular delivery, CAR engagement drives antigen-specific T-cell activation, cytokine release, and cytotoxic killing of CNS tumor cells, with multi-antigen targeting intended to mitigate antigen escape.
YES
DIRECT
CAR T cells engineered with an IL13-zetakine bind IL13Ralpha2 on tumor cells, triggering T-cell activation and perforin/granzyme-mediated cytolysis and apoptosis (with possible Fas–FasL/cytokine contributions).
Investigational immunotherapy; specific target/mechanism not disclosed in the registry.
LBL-024 is a tetravalent bispecific antibody that binds PD-L1 and 4-1BB. It blocks PD-L1 from engaging PD-1 to relieve checkpoint-mediated T-cell inhibition, while acting as a conditional 4-1BB agonist in PD-L1–positive tumor microenvironments to costimulate activated T cells and enhance antitumor cytotoxicity.
YES
INDIRECT
Blocks PD-L1/PD-1 to relieve inhibition and conditionally agonizes 4-1BB on T cells near PD-L1+ tumors, enhancing TCR-dependent T‑cell killing (perforin/granzyme) of PD-L1–expressing cells.
Investigational immunotherapy; specific target/mechanism not disclosed in the registry.
LBL-024 is a tetravalent bispecific antibody that binds PD-L1 and 4-1BB. It blocks PD-L1 from engaging PD-1 to relieve checkpoint-mediated T-cell inhibition, while acting as a conditional 4-1BB agonist in PD-L1–positive tumor microenvironments to costimulate activated T cells and enhance antitumor cytotoxicity.
NO
INDIRECT
LBL-024 binds 4-1BB on T cells and PD-L1 on tumor cells, blocking PD-L1/PD-1 and providing 4-1BB costimulation to activate T cells. The activated T cells then kill PD-L1–positive tumor cells; 4-1BB–expressing cells themselves are not killed.
An antibody–drug conjugate targeting Nectin-4 that delivers the cytotoxic payload MMAE (a microtubule inhibitor), leading to internalization, microtubule disruption, and tumor cell death in Nectin-4–expressing urothelial cancer cells.
A Nectin-4–targeted monoclonal antibody linked via a cleavable linker to the microtubule inhibitor MMAE; upon binding Nectin-4 on tumor cells, the ADC is internalized and MMAE is released to inhibit tubulin polymerization, causing G2/M arrest and apoptosis in Nectin-4–expressing cancer cells.
YES
DIRECT
The ADC binds Nectin-4 on target cells, is internalized, and releases MMAE after linker cleavage; MMAE inhibits tubulin polymerization, causing G2/M arrest and apoptosis of Nectin-4–expressing cells.
An antibody–drug conjugate targeting Nectin-4 that delivers the cytotoxic payload MMAE (a microtubule inhibitor), leading to internalization, microtubule disruption, and tumor cell death in Nectin-4–expressing urothelial cancer cells.
A Nectin-4–targeted monoclonal antibody linked via a cleavable linker to the microtubule inhibitor MMAE; upon binding Nectin-4 on tumor cells, the ADC is internalized and MMAE is released to inhibit tubulin polymerization, causing G2/M arrest and apoptosis in Nectin-4–expressing cancer cells.
NO
INDIRECT
The ADC binds Nectin-4 on tumor cells, is internalized, and releases MMAE, which binds beta-tubulin to inhibit microtubule polymerization causing G2/M arrest and apoptosis; beta-tubulin is not the targeted antigen determining cell killing.